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鼠李糖乳杆菌通过在体内增加闭合蛋白-1和肌球蛋白轻链激酶的表达,部分缓解肠道屏障功能障碍。

Lactobacillus rhamnosus alleviates intestinal barrier dysfunction in part by increasing expression of zonula occludens-1 and myosin light-chain kinase in vivo.

作者信息

Miyauchi E, Morita H, Tanabe S

机构信息

Graduate School of Biosphere Science, Hiroshima University, 1-4-4 Kagamiyama, Higashi-hiroshima, Hiroshima 739-8528, Japan.

出版信息

J Dairy Sci. 2009 Jun;92(6):2400-8. doi: 10.3168/jds.2008-1698.

Abstract

The effects of lactobacilli on impaired intestinal barrier function and paracellular permeability were evaluated in human epithelial Caco-2 cells treated with tumor necrosis factor-alpha and in mice with colitis induced by dextran sodium sulfate (DSS). Filter-grown Caco-2 monolayers were used as the intestinal epithelial model. Among the 4 lactobacilli studied, Lactobacillus rhamnosus OLL2838 most effectively suppressed barrier impairment and increased IL-8 secretion induced by tumor necrosis factor-alpha in Caco-2 cells; however, the conditioned medium from OLL2838 did not show any effect on barrier functions. The in vivo effects of OLL2838 on intestinal epithelial barrier function and colonic inflammation were assessed in DSS-induced colitis of BALB/c mice. Oral treatment with both live and heat-killed OLL2838 suppressed weight loss and recovered colon length. Additionally, barrier function was restored by the administration of live and heat-killed OLL2838 to the DSS-treated animals, which conferred protection against the increase in mucosal permeability associated with DSS-induced colitis. This may at least partially be because of the increased expression of zonula occludens-1 (4.8-fold) and myosin light-chain kinase (3.1-fold) in intestinal epithelial cells isolated from mice of the heat-killed OLL2838 group. Therefore, L. rhamnosus OLL2838 would be useful in the treatment of gastrointestinal diseases such as inflammatory bowel disease.

摘要

在经肿瘤坏死因子-α处理的人上皮Caco-2细胞以及由葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠中,评估了乳酸杆菌对受损肠屏障功能和细胞旁通透性的影响。滤膜培养的Caco-2单层细胞用作肠上皮模型。在所研究的4种乳酸杆菌中,鼠李糖乳杆菌OLL2838最有效地抑制了Caco-2细胞中由肿瘤坏死因子-α诱导的屏障损伤,并增加了IL-8的分泌;然而,OLL2838的条件培养基对屏障功能未显示任何作用。在BALB/c小鼠的DSS诱导的结肠炎中评估了OLL2838对肠上皮屏障功能和结肠炎症的体内作用。口服活的和热灭活的OLL2838均能抑制体重减轻并恢复结肠长度。此外,给DSS处理的动物施用活的和热灭活的OLL2838可恢复屏障功能,这为抵抗与DSS诱导的结肠炎相关的粘膜通透性增加提供了保护。这可能至少部分是由于从热灭活的OLL2838组小鼠分离的肠上皮细胞中紧密连接蛋白-1(4.8倍)和肌球蛋白轻链激酶(3.1倍)的表达增加。因此,鼠李糖乳杆菌OLL2838在治疗诸如炎症性肠病等胃肠道疾病中可能有用。

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